Abstract
Research has shown that spinal circuits have the capacity to adapt in response to training, nociceptive stimulation and peripheral inflammation. These changes in neural function are mediated by physiological and neurochemical systems analogous to those that support plasticity within the hippocampus (e.g., long-term potentiation and the NMDA receptor). As observed in the hippocampus, engaging spinal circuits can have a lasting impact on plastic potential, enabling or inhibiting the capacity to learn. These effects are related to the concept of metaplasticity. Behavioral paradigms are described that induce metaplastic effects within the spinal cord. Uncontrollable/unpredictable stimulation, and peripheral inflammation, induce a form of maladaptive plasticity that inhibits spinal learning. Conversely, exposure to controllable or predictable stimulation engages a form of adaptive plasticity that counters these maladaptive effects and enables learning. Adaptive plasticity is tied to an up-regulation of brain derived neurotrophic factor (BDNF). Maladaptive plasticity is linked to processes that involve kappa opioids, the metabotropic glutamate (mGlu) receptor, glia, and the cytokine tumor necrosis factor (TNF). Uncontrollable nociceptive stimulation also impairs recovery after a spinal contusion injury and fosters the development of pain (allodynia). These adverse effects are related to an up-regulation of TNF and a down-regulation of BDNF and its receptor (TrkB). In the absence of injury, brain systems quell the sensitization of spinal circuits through descending serotonergic fibers and the serotonin 1A (5HT 1A) receptor. This protective effect is blocked by surgical anesthesia. Disconnected from the brain, intracellular Cl- concentrations increase (due to a down-regulation of the cotransporter KCC2), which causes GABA to have an excitatory effect. It is suggested that BDNF has a restorative effect because it up-regulates KCC2 and re-establishes GABA-mediated inhibition.
Highlights
Research has shown that brain systems modulate the operation of spinal circuits
Studies of brain plasticity have uncovered processes that have a lasting impact on plastic potential, and we have suggested that this concept of metaplasticity has relevance to spinal function
We related this process to the development of central sensitization and Enhanced mechanical reactivity (EMR), and characterized these effects as examples of maladaptive plasticity
Summary
Research has shown that brain systems modulate the operation of spinal circuits. For example, afferent pain (nociceptive) signals can be inhibited, yielding an anti-nociception that attenuates both spinally mediated withdrawal and brain-mediated indices of pain (Fields, 2000). This R–O relation induces (through descending fibers) a lasting change in how a spinal circuit operates In this case, learning is mediated by the brain and the consequence of this process (the memory) is stored within the spinal cord. An extended exposure to fixed spaced shock engages a protective mechanism that counters the adverse effects of VIS (Baumbauer et al, 2009, 2012; Baumbauer and Grau, 2011) These effects are lasting (24 h or longer), involve a form of NMDAR-mediated plasticity, and require protein synthesis We take this position because we have yet to elucidate the relative role of these phenomena and because we assume that neural plasticity may be mediated by a host of mechanisms
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